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Gene 'switch' reverses cancer in common childhood leukaemia
Date:6/17/2014

ight on the function of Pax5, which was one of about 100 genes known to 'suppress' human tumours. "When these tumour suppressor genes are inactivated by changes to the DNA, cancers start to develop," Dr Dickins said.

"This work shows how inactivating the tumour suppressor gene Pax5 contributes to B-ALL development and how leukaemia cells become 'addicted' to low Pax5 levels to continue proliferating. Even though the B-ALL cells have multiple genetic mutations, simply reactivating Pax5 causes tumour cells to resume normal development and lose their cancerous properties."

Dr Dickins said forcing B-ALL cells to resume their normal development could provide a new strategy for treating leukaemia. "While B-ALL has a relatively good prognosis compared with other cancers, current treatments can last years and have major side-effects. By understanding how specific genetic changes drive B-ALL, it may be possible to develop more specific treatments that act faster with fewer side-effects."

However Dr Dickins said that genes that are lost in tumour cells are not traditionally drug targets. "It is very difficult to develop drugs that restore the function of genes that are lost during cancer development," Dr Dickins said. "However by understanding the mechanisms by which Pax5 loss causes leukaemia, we can begin to look at ways of developing drugs that could have the same effect as restoring Pax5 function."

The genetic switch technology used to study Pax5 could also be used to understand 'tumour suppressor' genes in other cancers, he said.


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Contact: Liz Williams
williams@wehi.edu.au
61-428-034-089
Walter and Eliza Hall Institute
Source:Eurekalert  

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